THE METHANOL SEED EXTRACT OF GARCINIA KOLA ATTENUATED ANGIOTENSIN II- AND LIPOPOLYSSACHARIDE-INDUCED VASCULAR SMOOTH MUSCLE CELL PROLIFERATION AND NITRIC OXIDE PRODUCTION
THE METHANOL SEED EXTRACT OF GARCINIA KOLA ATTENUATED ANGIOTENSIN II- AND LIPOPOLYSSACHARIDE-INDUCED VASCULAR SMOOTH MUSCLE CELL PROLIFERATION AND NITRIC OXIDE PRODUCTION
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DOI：
10.1515/macvetrev-2016-0079
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发表时间：
2016-10-01
影响因子：
0.4
通讯作者：
Yakubu, Momoh A.
中科院分区：
文献类型：
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作者：
Adedapo, Adeolu A.;Omobowale, Temidayo O.;Yakubu, Momoh A.
在世界各地，心血管疾病是健康状况不佳和过早死亡的一个危险因素，其诱发因素包括年龄、性别、吸烟、缺乏身体活动、过度饮酒、不健康饮食、肥胖、心血管疾病家族史、高血压、糖尿病、高脂血症、社会心理因素、贫穷和低教育程度以及空气污染。可以设想，能够遏制这一趋势的草药产品将大有裨益。Garcinia kola (GK)，也被称为苦kola，就是这样的植物之一。苦可乐通常被用作社交小吃，在一些文化场所提供给客人，它被用于治疗喉炎、一般炎症、支气管炎、病毒感染和糖尿病。在血管紧张素II （Ang II）和脂多糖诱导NO生成的细胞培养条件下，研究了藤黄甲醇籽提取物对血管平滑肌细胞（VSMCs）增殖的影响。在脂多糖（100 μ g/ml）和血管紧张素II (10（-8)-10(-6)M）治疗前后，将融合型VSMCs暴露于GK（25、50和100 μ g/ml）。MTT法检测细胞增殖，Griess法检测NO生成。血管紧张素II(10（-8), 10(-6)）或LPS均可显著增强VSM细胞的增殖，LPS可显著增加一氧化氮（NO）的生成。GK（25、50和100 μ g/ml）处理能减弱VSM细胞的增殖。结果表明，GK可能抑制有丝分裂原激活的血管细胞生长，并可能抑制对LPS的炎症反应。因此，GK可能在以细胞增殖和炎症反应为特征的条件下有用。
All over the world, cardiovascular diseases are a risk factor for poor health and early death with predisposing factors to include age, gender, tobacco use, physical inactivity, excessive alcohol consumption, unhealthy diet, obesity, family history of cardiovascular disease, hypertension, diabetes mellitus, hyperlipidemia, psychosocial factors, poverty and low educational status, and air pollution. It is envisaged that herbal products that can stem this trend would be of great benefit. Garcinia kola (GK), also known as bitter kola is one of such plants. Generally used as a social snack and offered to guests in some cultural settings, bitter kola has been indicated in the treatment of laryngitis, general inflammation, bronchitis, viral infections and diabetes. In this study, the effects of methanol seed extract of Garcinia kola on the proliferation of Vascular Smooth Muscle Cells (VSMCs) in cell culture by Angiotensin II (Ang II) and LPS-induced NO production were carried out. Confluent VSMCs were exposed to GK (25, 50 and 100 mu g/ml) before or after treatment with lipopolyssacharide (100 mu g/ml), and Angiotensin II (10(-8)-10(-6)M). Cellular proliferation was determined by MTT assay and NO production by Griess assay. Treatment with Angiotensin II (10(-8), 10(-6)) or LPS significantly enhanced proliferation of VSM cells while LPS significantly increased nitric oxide (NO) production. Treatment with GK (25, 50 & 100 mu g/ml) attenuated VSM cell proliferation. The results indicate that GK has potential to inhibit mitogen activated vascular cell growth and possibly inhibit inflammatory responses to LPS. Thus GK may be useful in condition that is characterized by cellular proliferation and inflammatory responses.